Zoology 523: Neurobiology Exam 3 ACTUAL UPDATED Questions and CORRECT
Answers
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Terms in this set (59)
How do AMPA and NDMA glutamate receptors differ AMPA receptors are a Glu-gated Na+/K+ channel that depolarize the cell when
from each other? opened. NDMA channels open in response to the Glu and depolarization (20-30
mV from rest). NDMA channels let in lots of Ca++
Where do the examples of LTP and LTD we examined Pyramidal cells in the CA1 region of the hippocampus
take place?
What are the different time courses of Memory? Short term, working, long-term
What are the different ways memory is expressed? Declarative/Explicit, Nondeclarative/Implicit
Types of Memory acquisition Associative: associating two different stimuli
Non-associative: Habituation/Depression, Sensitization/Potentiation
Where is declarative memory found? Across the cerebral cortex, early phases take place in Hippocampus/medial
temporal cortex
Explain Heterosynaptic/Associative LTP Weak tetanus of one synapse does not give LTP, simultaneous tetanus of both
does
How do you measure LTP? What are you looking at that Measure the EPSP response to weak input, deliver strong tetanic stimulation,
has "potentiated"? measure EPSP response to original weak input.
What postsynaptic events lead from a strong (tetanic) Glu binds to AMPA channels, cell depolarizes, NMDA channels open, Ca++ enters
stimulus in the presynaptic neuron to the fast the cell, Ca++ activates Calmodulin (CaM), CaM binds CAMKII, CAMKII
(milliseconds to seconds) physiological changes of LTP in phosphorylates AMPA receptors, trafficks AMPA channels to synapse membrane
pyramidal cells in the CA1 region of the hippocampus? (From vesicles and membrane)
What would you expect to happen to LTP if you applied APV applied after the tetanus you still get LTP because Ca++ pathways have
APV to the pyramidal cell 5 minutes after the tetanus? activated, applied before the stimulus, the Ca++ does not enter the cell so not LTP
What if you instead applied the APV before the stimulus? takes place
Why does the early phase of LTP last so long? What 1. Greater depolarization activates more NMDA channels, additional Ca++
processes tend to lock the postsynaptic cell into a channels and imports AMPA channels
potentiated state? 2. Ca++ triggers release of Ca++ in smooth ER
3. CAMKII activates/phosphorylates CAMKII
What are silent synapses in regards to memory? Synapses with few AMPA receptors
How does the early phase of LTP differ from the late New proteins need to be synthesized, the synapse enlarges, requires cAMP to
phase? activate PKA, to activate CREB
, Early phase LTP Ca++ Pathway Ca++ activates CaM, CaM activates CAMKII, CAMKII phosphorylates AMPA and
trafficks channels to synapse
Late phase LTP Ca++ Pathway Ca++ activates Adenylyl cyclase, turns ATP to cAMP, cAMP activates PKA, PKA
phosphorylates CREB transcription factor, phosphorylates other things
Proposed Presynaptic feedback signals NO (Nitric oxide), BDNF (brain-derived neurotrophic factor), synapse building
proteins
What is the chain of events that leads from a weak tetanus Weak tetanus means less Ca++ enters cell, activates phosphatase, removes
to LTD? Why is the outcome the opposite of LTP? phosphate from AMPA, removes AMPA from synapse
How does Ca++ effect synaptic competition in LTP Ca++ can diffuse from the synapse of LTP and cause LTD in a neighboring synapse
What are some different types of human memory? Are Declarative (explicit) memory is routed through the Hippocampus.
there any that are not reliant on the hippocampus? Nondeclarative (implicit) memory involves central pattern generators. Does not
involve the hippocampus
What stimulates PKA in the siphon sensory neuron of Serotonin activates GPCRs, activate adenylyl cyclase, cAMP, PKA.
Aplysia? What effects does PKA have in the presynaptic PKA closes K+ channels, opens Ca++, activates CREB (transcription for bigger
terminal? synapses)
How does Aplysia CPEB (cytoplasmic polyadenylation Aplysia CPEB in active form acts as a prion, converts others into the active shape.
binding protein) lock in long term memories?
What are two ways that PKA affects the outcome of an PKA shuts down K+ channels (AP lasts longer), Opens Ca++ channels (more
action potential travelling down Aplysia siphon sensory synaptic release)
neurons?
Why does stretching the spindle fiber in a muscle cause Stretch Reflex:
relaxation in the antagonist muscle? What circuit is used? Stretching muscle spindle stimulates sensory neuron, sensory neuron excites
motoneurons to stretched muscle to contract, sensory neuron also excites
interneuron that inhibits motoneurons to antagonist muscle
What evidence indicates that most repetitive behaviors Some deafferented neurons still fire with sensory input
are not simply the result of repeated reflexes?
What is the definition of a central pattern generator? A Central Pattern Generator provides repetitive motor neuron output without
input from sensory neurons.
What are the two main sources of rhythmic output in 1) circuitry between neurons
central pattern generators? 2) intrinsic rhythmic properties of "bursting pacemaker" neurons
What does it mean to be deafferented? Sensory input has been removed
How is reciprocal inhibition between neurons used to Neuron A will inhibit neuron B, until A gets worn out and the B inhibits A. Stimulus
reinforce the patterned firing of central pattern from other neurons such central pattern generators may be needed to get these
generators? And what else might be needed to make neurons to fire.
these neurons fire action potentials?
Answers
C
Terms in this set (59)
How do AMPA and NDMA glutamate receptors differ AMPA receptors are a Glu-gated Na+/K+ channel that depolarize the cell when
from each other? opened. NDMA channels open in response to the Glu and depolarization (20-30
mV from rest). NDMA channels let in lots of Ca++
Where do the examples of LTP and LTD we examined Pyramidal cells in the CA1 region of the hippocampus
take place?
What are the different time courses of Memory? Short term, working, long-term
What are the different ways memory is expressed? Declarative/Explicit, Nondeclarative/Implicit
Types of Memory acquisition Associative: associating two different stimuli
Non-associative: Habituation/Depression, Sensitization/Potentiation
Where is declarative memory found? Across the cerebral cortex, early phases take place in Hippocampus/medial
temporal cortex
Explain Heterosynaptic/Associative LTP Weak tetanus of one synapse does not give LTP, simultaneous tetanus of both
does
How do you measure LTP? What are you looking at that Measure the EPSP response to weak input, deliver strong tetanic stimulation,
has "potentiated"? measure EPSP response to original weak input.
What postsynaptic events lead from a strong (tetanic) Glu binds to AMPA channels, cell depolarizes, NMDA channels open, Ca++ enters
stimulus in the presynaptic neuron to the fast the cell, Ca++ activates Calmodulin (CaM), CaM binds CAMKII, CAMKII
(milliseconds to seconds) physiological changes of LTP in phosphorylates AMPA receptors, trafficks AMPA channels to synapse membrane
pyramidal cells in the CA1 region of the hippocampus? (From vesicles and membrane)
What would you expect to happen to LTP if you applied APV applied after the tetanus you still get LTP because Ca++ pathways have
APV to the pyramidal cell 5 minutes after the tetanus? activated, applied before the stimulus, the Ca++ does not enter the cell so not LTP
What if you instead applied the APV before the stimulus? takes place
Why does the early phase of LTP last so long? What 1. Greater depolarization activates more NMDA channels, additional Ca++
processes tend to lock the postsynaptic cell into a channels and imports AMPA channels
potentiated state? 2. Ca++ triggers release of Ca++ in smooth ER
3. CAMKII activates/phosphorylates CAMKII
What are silent synapses in regards to memory? Synapses with few AMPA receptors
How does the early phase of LTP differ from the late New proteins need to be synthesized, the synapse enlarges, requires cAMP to
phase? activate PKA, to activate CREB
, Early phase LTP Ca++ Pathway Ca++ activates CaM, CaM activates CAMKII, CAMKII phosphorylates AMPA and
trafficks channels to synapse
Late phase LTP Ca++ Pathway Ca++ activates Adenylyl cyclase, turns ATP to cAMP, cAMP activates PKA, PKA
phosphorylates CREB transcription factor, phosphorylates other things
Proposed Presynaptic feedback signals NO (Nitric oxide), BDNF (brain-derived neurotrophic factor), synapse building
proteins
What is the chain of events that leads from a weak tetanus Weak tetanus means less Ca++ enters cell, activates phosphatase, removes
to LTD? Why is the outcome the opposite of LTP? phosphate from AMPA, removes AMPA from synapse
How does Ca++ effect synaptic competition in LTP Ca++ can diffuse from the synapse of LTP and cause LTD in a neighboring synapse
What are some different types of human memory? Are Declarative (explicit) memory is routed through the Hippocampus.
there any that are not reliant on the hippocampus? Nondeclarative (implicit) memory involves central pattern generators. Does not
involve the hippocampus
What stimulates PKA in the siphon sensory neuron of Serotonin activates GPCRs, activate adenylyl cyclase, cAMP, PKA.
Aplysia? What effects does PKA have in the presynaptic PKA closes K+ channels, opens Ca++, activates CREB (transcription for bigger
terminal? synapses)
How does Aplysia CPEB (cytoplasmic polyadenylation Aplysia CPEB in active form acts as a prion, converts others into the active shape.
binding protein) lock in long term memories?
What are two ways that PKA affects the outcome of an PKA shuts down K+ channels (AP lasts longer), Opens Ca++ channels (more
action potential travelling down Aplysia siphon sensory synaptic release)
neurons?
Why does stretching the spindle fiber in a muscle cause Stretch Reflex:
relaxation in the antagonist muscle? What circuit is used? Stretching muscle spindle stimulates sensory neuron, sensory neuron excites
motoneurons to stretched muscle to contract, sensory neuron also excites
interneuron that inhibits motoneurons to antagonist muscle
What evidence indicates that most repetitive behaviors Some deafferented neurons still fire with sensory input
are not simply the result of repeated reflexes?
What is the definition of a central pattern generator? A Central Pattern Generator provides repetitive motor neuron output without
input from sensory neurons.
What are the two main sources of rhythmic output in 1) circuitry between neurons
central pattern generators? 2) intrinsic rhythmic properties of "bursting pacemaker" neurons
What does it mean to be deafferented? Sensory input has been removed
How is reciprocal inhibition between neurons used to Neuron A will inhibit neuron B, until A gets worn out and the B inhibits A. Stimulus
reinforce the patterned firing of central pattern from other neurons such central pattern generators may be needed to get these
generators? And what else might be needed to make neurons to fire.
these neurons fire action potentials?
